At the time of infection of an E. coli cell with a T4 bacteriophage, that cell is presented with two sets of genetic instructions dictating two completely different pathways of metabolic activity. At least in the case of the commonly studied E. coli strains grown under standard laboratory conditions, such T4-infected cells respond invariably to the dictations of the viral genome. This genetic takeover of the host cell's metabolic machinery is the basis for the pathogenicity of viruses. Phage T4-infected E. coli provides a favorable system with which to study the genetics of such host-parasite interrelationships. Starting with multiple mutant strains of phage T4 which fail to induce the three known T4-induced modifications of the functional host nucleoid, namely, DNA degradation, nuclear disruption, and unfolding of the folded genomes, we propose to construct multiple mutant strains (by inducing new mutations and crossing in known mutations) that do not shut off host (1) DNA synthesis, (2) RNA synthesis, or (3) protein synthesis. After the addition of each mutation, we will cary out comparative biochemical analyses of cells infected with the new multiple mutant and of cells infected with its isogenic parent strain. Particular emphasis will be given to identifying the genes coding for the proteins added to the ribosomes after T4 infection. In this way, we should be able to catalog all the genes and gene-products involved in the shutoff of host DNA, RNA, and protein synthesis.